Attenuation of Interleukin-8 Expression in C6-deficient Rabbits After Myocardial Ischemia/Reperfusion

Kilgore, Kenneth S.; Park, James; Tanhehco, Elaine J.; Booth, Erin A.; Marks, Rebecca A.; Lucchesi, Benedict R.

doi:10.1006/jmcc.1997.0573

Cited by 57 publications

(32 citation statements)

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“…TNF-a deficient mice undergoing experimental infarction protocols exhibit decreased chemokine and adhesion molecule expression suggesting an important role for TNF-a in mediating the post-infarction chemokine response [44]. Kilgore and co-workers [45] reported an attenuated IL-8 response accompanied by decreased neutrophil infiltration in C6-deficient rabbits, suggesting that the cytolytic membrane Vol. 53, 2004 Chemokines in myocardial ischemia 587 attack complex plays an important role in regulating expression of the chemokine in the infarct.…”

Section: Chemokine Expression In Experimental Models Of Myocardial Inmentioning

confidence: 99%

Chemokines in the ischemic myocardium: from inflammation to fibrosis

2004

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Myocardial infarction is associated with an inflammatory response leading to leukocyte recruitment, healing and formation of a scar. Members of the chemokine superfamily are rapidly induced in the infarcted myocardium and may critically regulate the post-infarction inflammatory response. CXCL8/Interleukin (IL)-8 is upregulated in the infarcted area and may induce neutrophil infiltration. In addition, mononuclear cell chemoattractants, such as the CC chemokines CCL2/Monocyte Chemoattractant Protein (MCP)-1, CCL3/Macrophage Inflammatory Protein (MIP)1alpha, and CCL4/MIP-1beta are expressed in the ischemic area, and may regulate monocyte and lymphocyte recruitment. However, chemokines may have additional effects on healing infarcts beyond their leukotactic properties. The CXC chemokine CXCL10/Interferon-y inducible Protein (IP)-10, a potent angiostatic factor with antifibrotic properties, is induced in the infarct and may prevent premature angiogenesis and fibrous tissue deposition, until the infarct is debrided and provisional matrix necessary to support granulation tissue ingrowth is formed. Chemokine induction in the infarct is transient, suggesting that inhibitory mediators (such as transforming growth Factor (TGF)-beta) may be activated suppressing chemokine synthesis and leading to resolution of inflammation and transition to fibrosis. Brief repetitive ischemia in mice also results in chemokine upregulation followed by suppression of chemokine synthesis and interstitial fibrosis, in the absence of myocardial infarction. Chemokine expression may play a role in the pathogenesis of non-infarctive ischemic cardiomyopathy, where early ischemia-induced chemokine expression may be followed by activation of inhibitory mediators that suppress inflammation, but induce fibrosis.

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Section: Chemokine Expression In Experimental Models Of Myocardial Inmentioning

confidence: 99%

Chemokines in the ischemic myocardium: from inflammation to fibrosis

2004

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“…Interestingly, abolition of C9 deposition in the central nervous system after CVF treatment has also been reported in acute antibody-mediated demyelinating experimental allergic encephalomyelitis. 12 In addition, Kilgore and coworkers 39 found that the infarct size is significantly reduced in hearts from C6-deficient rabbits in their ischemia/reperfusion model and that hereditary C6-deficient rabbits are not able to form MAC. They also reported that N-acetylheparin, an inhibitor of complement activation, reduces MAC content and myocardial infarct volume in the myocardial ischemia/reperfusion model.…”

Section: Et Al Complement Depletion and Brain Edema In Ichmentioning

confidence: 99%

Systemic Complement Depletion Diminishes Perihematomal Brain Edema in Rats

Hua

Keep

et al. 2001

Stroke

121

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Background and Purpose-The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH. Methods-Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complementdepleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 L) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-␣ (TNF-␣) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-␣ levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase.

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“…Complement activation with increased systemic levels of the anaphylatoxins C3a and C5a occurs in patients with severely ischemic limbs and respiratory failure [80]. In C6-deficient animal model, an attenuated IL-8 response accompanied by decreased neutrophil infiltration was noted [81]. C5-deficient mice exhibited decreased lung and liver injury after lower torso ischemia, that was restored after reconstitution with wild-type serum [43] and administration of a specific C5a receptor antagonist abolished upregulation of the CXC-chemokine family and led to reduced neutrophil infiltration [82].…”

Section: Endothelial Cell-dysfunction and Leukocyte Adhesionmentioning

confidence: 96%

Ischemia-Reperfusion Injury

Dorweiler

Pruefer²,

Andrási³

et al. 2007

Eur J Trauma Emerg Surg

114

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The term ischemia-reperfusion injury describes the experimentally and clinically prevalent finding that tissue ischemia with inadequate oxygen supply followed by successful reperfusion initiates a wide and complex array of inflammatory responses that may both aggravate local injury as well as induce impairment of remote organ function. Conditions under which ischemia-reperfusion injury is encountered include the different forms of acute vascular occlusions (stroke, myocardial infarction, limb ischemia) with the respective reperfusion strategies (thrombolytic therapy, angioplasty, operative revascularization) but also routine surgical procedures (organ transplantation, free-tissue-transfer, cardiopulmonary bypass, vascular surgery) and major trauma/shock. Since the first recognition of ischemia-reperfusion injury during the 1970s, significant knowledge has accumulated and the purpose of this review is to present an overview over the current literature on the molecular and cellular basis of ischemia-reperfusion injury, to outline the clinical manifestations and to compile contemporary treatment and prevention strategies. Although the concept of reperfusion injury is still a matter of debate, it is corroborated by recent and ongoing clinical trials that demonstrated ischemic preconditioning, inhibition of sodium-hydrogen-exchange and administration of adenosine to be effective in attenuating ischemia-reperfusion injury.

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Attenuation of Interleukin-8 Expression in C6-deficient Rabbits After Myocardial Ischemia/Reperfusion

Cited by 57 publications

References 0 publications

Chemokines in the ischemic myocardium: from inflammation to fibrosis

Chemokines in the ischemic myocardium: from inflammation to fibrosis

Systemic Complement Depletion Diminishes Perihematomal Brain Edema in Rats

Ischemia-Reperfusion Injury

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